Multiple systems organ failure remains the common pathway to death in the intensively supported multiple trauma patient. The mechanisms are undoubtedly very complex. However, a logical case can be made for a significant, at present untreated, component produced by a muscle fuel deficit with consumption of essential branched chain amino acids. This could produce the reduced protein synthesis, the altered cerebral function, the systemic arteriovenous shunting, and the terminal biventricular failure unresponsive to positive inotropic agents. We propose to investigate this hypothesis in a number of projects. The project by Bernardis is to explore the functional neuroanatomy of the response to trauma and sepsis. Cerra's project explores the circulatory consequences of various muscle fuels. Border's project explores the mechanisms and systemic metabolic consequences of various muscle fuels. McMenamy's project is an animal exploration of abnormal cycles related to the proposed muscle fueld deficit and a search for additional unrecognized metabolic components of this problem. VanOss explores the phagocytic changes and their mechanisms in these patients. Spangler's group utilizes the data we have obtained to build model systems and evaluate them for new analyses of the data and the requirement for new types of data.